EU Risk Assessment Summary Report

EUROPEAN COMMISSION
JOINT
RESEARCH
CENTRE
Institute for Health and Consumer Protection
European Chemicals Bureau
I-21020 Ispra (VA) Italy
ACRYLONITRILE
CAS No: 107-13-1
EINECS No: 203-466-5
Summary Risk Assessment Report
2004
Special Publication I.03.157
ACRYLONITRILE
CAS No: 107-13-1
EINECS No: 203-466-5
SUMMARY RISK ASSESSMENT REPORT
Final report 2004
Ireland
The risk assessment of acrylonitrile has been prepared by Ireland on behalf of the European
Union. The scientific work contained in the report has been prepared by the Hazardous
Substances Assessment Unit of the Health and Safety Authority.
Contact:
Hazardous Substances Assessment Unit
Health and Safety Authority,
10, Hogan Place,
Dublin 2
Mrs Roisin McEneany, Dr Majella Cummins
Tel:
353-1-6147000
Fax:
353-1-6147017
E-mail: [email protected]
Date of Last Literature Search:
Review of report by MS Technical Experts finalised:
Final report:
© European Communities, 2004
1999
2000
2004
PREFACE
This report provides a summary, with conclusions, of the risk assessment report of the
substance acrylonitrile that has been prepared by Ireland in the context of Council Regulation
(EEC) No. 793/93 on the evaluation and control of existing substances.
For detailed information on the risk assessment principles and procedures followed, the
underlying data and the literature references the reader is referred to the comprehensive Final
Risk Assessment Report (Final RAR) that can be obtained from the European Chemicals
Bureau1. The Final RAR should be used for citation purposes rather than this present
Summary Report.
1
European Chemicals Bureau – Existing Chemicals – http://ecb.jrc.it
III
CONTENTS
1 GENERAL SUBSTANCE INFORMATION..........................................................................................
3
1.1 IDENTIFICATION OF THE SUBSTANCE..................................................................................
3
1.2 PHYSICO-CHEMICAL PROPERTIES ........................................................................................
3
1.3 CLASSIFICATION ..........................................................................................................................
4
2 GENERAL INFORMATION ON EXPOSURE .....................................................................................
5
3 ENVIRONMENT ......................................................................................................................................
6
3.1 ENVIRONMENTAL EXPOSURE..................................................................................................
6
3.2 EFFECTS ASSESSMENT ...............................................................................................................
8
3.3 RISK CHARACTERISATION .......................................................................................................
9
4 HUMAN HEALTH ...................................................................................................................................
11
4.1 HUMAN HEALTH (TOXICITY) ...................................................................................................
4.1.1 Exposure assessment ...............................................................................................................
4.1.2 Effects assessment ...................................................................................................................
4.1.3 Risk characterisation................................................................................................................
11
11
13
15
4.2 HUMAN HEALTH (PHYSICO-CHEMICAL PROPERTIES) ...................................................
17
5 RESULTS...................................................................................................................................................
18
5.1 ENVIRONMENT..............................................................................................................................
18
5.2 HUMAN HEALTH...........................................................................................................................
5.2.1 Human health (toxicity) ...........................................................................................................
5.2.2 Human health (risks from physico-chemical properties) .........................................................
18
18
19
Appendix A Local PEC and other emission parameters for surface water for acrylonitrile production
plants in Europe ..........................................................................................................................
Appendix B Local PEC and other emission parameters for surface water for acrylonitrile processing
plants in Europe ..........................................................................................................................
Appendix C Local PEC and other emission parameters to air for acrylonitrile production plants in Europe.
Appendix D Local PEC and other emission parameters to air for acrylonitrile processing plants in Europe .
21
23
25
27
TABLES
Table 1.1 Summary of physico-chemical properties .....................................................................................
Table A.1 Local PEC and other emission parameters for surface water for acrylonitrile production plants in
Europe ...........................................................................................................................................
Table B.1 Local PEC and other emission parameters for surface water for acrylonitrile processing plants in
Europe ...........................................................................................................................................
Table C.1 Local PEC and other emission parameters to air for acrylonitrile production plants in Europe....
Table D.1 Local PEC and other emission parameters to air for acrylonitrile processing plants in Europe ....
1
3
21
23
25
27
1
GENERAL SUBSTANCE INFORMATION
1.1
IDENTIFICATION OF THE SUBSTANCE
CAS Number:
EINECS Number:
IUPAC Name:
Synonyms:
Molecular weight:
Molecular formula:
Structural formula:
1.2
107-13-1
203-466-5
2-propenenitrile
Vinyl cyanide, cyanoethylene, acrylonitrile
53.06
C3H3N
CH2 = CH - CN
PHYSICO-CHEMICAL PROPERTIES
Table 1.1 Summary of physico-chemical properties
Property
Value
Physical state
Colourless liquid
Solidifying Point
- 83.55°C * + 0.5°C
Boiling point
77.3°C *
Relative Density
0.8060 at 20°C
Vapour Pressure
115 hPa at 20°C
133.3 hPa at 22.8°C *
Surface tension
27.3 mN/m at 24°C
Water solubility
73.5 g/l at 20°C *
Partition coefficient (log Pow)
0.25 *
Flash point
0°C (open cup method)
-5°C (open cup method)
Autoflammability
481°C
* value used in the assessment of environmental exposure in this report
3
EU RISK ASSESSMENT - ACRYLONITRILE
1.3
SUMMARY, 2004
CLASSIFICATION
Classification and labelling according to the 26th ATP of Directive 67/548/EEC2:
Classification
F; R11
Carc. Cat.2; R45
T; R23/24/25
Xi; R37/38-41
Highly flammable
May cause cancer
Also toxic by inhalation, in contact with skin and if swallowed
Irritating to respiratory system and skin. Risks of serious
damages to eyes
May cause sensitisation by skin contact
Dangerous for the environment, toxic to aquatic organisms,
may cause long-term adverse effects in the aquatic environment
R43
N; R51-53
Notes: D, E
Labelling
F; T; N
R 45-11-23/24/25-37/38-41-43-51/53
S 9-16-53-45-61
Specific concentration limits
C > 20%
10%<C<20%
5%<C<10%
1%<C< 5%
0.2%<C< 1%
0.1%<C<0.2%
2
T; R45-23/24/25-37/38-41-43
T; R45-23/24/25-41-43
T; R45-23/24/25-36-43
T; R45-23/24/25-43
T; R45-20/21/22
T; R45
The classification of the substance is established by Commission Directive 2000/32/EC of 19 May 2000 adapting to technical
progress for the 26th time Council Directive 67/548 on the approximation of the laws, regulations and administrative provisions
relating to the classification, packaging and labelling of dangerous substances.
4
2
GENERAL INFORMATION ON EXPOSURE
Production of acrylonitrile in the European Union over the period 1994-1996 was in excess of
1,250,000 tonnes per annum (source PCI World Acrylonitrile Report, 1996). Acrylonitrile is
produced from ammonia and propylene via catalytic ammoxidation in a closed system. It is
used almost exclusively as a monomer in the production of polymeric materials, with some
use as a precursor in the production of acrylamide and adiponitrile. Approximately 52% of the
total EU production of acrylonitrile is used for the production of acrylic and modacrylic
textile fibres, used in clothing and domestic furnishings. Production of acrylonitrilebutadiene-styrene (ABS) and styrene-acrylonitrile (SAN) plastics, used in automotive parts,
household appliances, pipe fittings, containers for food, etc. accounts for 15% of use, while a
further 15% is used in the production of acrylamide and adiponitrile and 18% for other uses,
including production of nitrile rubber and other polymeric materials.
At the time that data were collected for the purposes of this risk assessment, in 1994–1996,
acrylonitrile was produced by 7 manufacturers at 8 sites in the European Union, located in
Germany, Italy, Netherlands, Spain and the United Kingdom. Although production takes
place in closed systems in a largely continuous process, start-up, shut-down, product recovery
and purification steps result in some release of acrylonitrile to air or water. Production wastes
are however either incinerated, or treated by for example gas scrubbing of emissions followed
by release of scrubber washes to wastewater, thus significantly reducing the environmental
emissions. Tank breathing during storage is a further source of releases to atmosphere.
Data provided by the PCI World Acrylonitrile and Derivatives Supply/Demand Report (1996)
indicated that at that time there were 11 major facilities producing acrylic fibres throughout
Western Europe, two of which ceased production in 1996/97, 13 facilities producing
ABS/SAN plastics, 10 facilities producing nitrile:butadiene copolymers, 3 facilities producing
acrylamide and 1 producing adiponitrile. Limited (drum) quantities of acrylonitrile are used
by a number of small companies in Europe. The estimate for drummed product for the whole
European Union market is less than 1,000 tonnes, on a total production tonnage of
1,250,000 tonnes, or less than 0.1%. As for production, polymerisation of acrylonitrile is
carried out in largely closed systems, using broadly similar polymerisation processes,
however start-up, shut-down, product recovery and washing steps result in some release of
acrylonitrile to air or water. Following polymerisation, unreacted monomer is recovered and
recycled to the reactor.
Subsequent processing steps involving acrylonitrile in polymerised form, e.g. drying, dyeing
of fibres or use in textile manufacture, shaping of acrylonitrile plastics and rubbers, are
assumed to result in relatively minor releases of free acrylonitrile compared with the initial
polymerisation and processing steps, given the low content of residual monomer.
Releases of acrylonitrile within production and processing facilities can result in exposure of
workers, while releases to atmosphere and water can lead to exposure of the environment and
consequently to man exposed via the environment. Vehicle exhausts have been reported to
represent a significant source of diffuse emissions of acrylonitrile to air, while cigarette
smoke represents a minor source. Consumers may potentially be exposed via use or wearing
of materials which may contain a small percentage of unreacted monomer, or via the food
which is packaged in containers made from acrylonitrile derived plastics. In practice, data
gathered for the risk assessment report indicates that consumer exposure is extremely low.
5
3
ENVIRONMENT
3.1
ENVIRONMENTAL EXPOSURE
Exposure of the aquatic compartment to acrylonitrile may occur as a result of release to water
during production of monomer, polymerisation of monomer to give acrylonitrile polymers,
further processing of polymer to give polymeric products, use and, ultimately, disposal of the
polymeric products. Exposure on a local scale is to a limited (multiple) number of point
sources involved in the large-scale production of acrylonitrile and/or further processing of
acrylonitrile polymers. Exposure to acrylonitrile as a result of disposal of polymeric products
to landfill for example, with subsequent release to the aquatic environment, is considered to
be insignificant compared with manufacturing point sources. Emissions from vehicle exhausts
and other diffuse sources, as mentioned in Section 2 are largely to atmosphere rather than the
aquatic compartment. Tank breathing during storage is a further source of releases to
atmosphere. Modelling of environmental distribution using measured values for vapour
pressure, water solubility, log Pow and other physicochemical properties and a value of
9.62 Pa/m3/mol for Henry's law constant indicates that the predicted major environmental
compartment for acrylonitrile is air, with a smaller proportion entering the aqueous
compartment and negligible quantities being predicted for other compartments.
The total releases from all currently operational production and processing plants provide a
figure of approximately 400 tonnes per annum acrylonitrile released to water, on a production
volume of approximately 1,250,000 tonnes per annum. The point source releases to air for
continental releases at a European level have been estimated to total 900 tonnes per annum.
Indirect emissions due to e.g. vehicle exhausts may contribute as much as 2,400 tonnes per
annum of acrylonitrile, although this is considered to represent a worst-case analysis.
In relation to exposure assessment for the aquatic environment, the currently operational
production and further processing companies can be divided into three groups:
1. Facilities with dedicated industrial wastewater treatment plants,
2. Two facilities discharging into a municipal wastewater treatment plant following
preliminary physicochemical treatment to recover acrylonitrile from waste,
3. Facilities discharging directly into the aquatic environment (river/marine/estuarine)
without biotreatment.
In the case of group (1), which represents a large proportion of total sites (33 out of a total of
43), the results of laboratory-scale simulation studies and other information indicate that
acrylonitrile may be regarded as readily biodegradable in this situation. In the case of groups
(2) and (3) it is regarded as inherently biodegradable. Following release to the environment,
acrylonitrile is thus degraded in water, and also in the atmosphere and in soil. Photolytic
degradation in water has also been reported. In relation to atmospheric degradation the
.
published rate constant for the reaction of acrylonitrile with OH of 3.2.10-12cm/mol/s has
been used in EUSES, representing an estimated half-life of 5 days in the troposphere.
Experimental data for biodegradation provide values for the half-life ranging from 2 days in a
fully acclimated system to 15 days in a ready biodegradability test in seawater and 30 days in
a standard ready biodegradability test. Transfer of acrylonitrile from the aqueous to the
atmospheric compartment can potentially arise as a consequence of volatilisation and air
stripping from WWTP, given the relatively high vapour pressure of acrylonitrile. However
this is counterbalanced by its high water solubility.
6
CHAPTER 3. ENVIRONMENT
Bioaccumulation of acrylonitrile is not anticipated, given experimentally derived values of
0-0.3 for the log Kow, and a bioconcentration factor (BCF) of 1.0 has been calculated from
the known water solubility of acrylonitrile. EUSES calculates a BCF for fish and aquatic biota
of 1.41 L/kg.
PEC calculations
PECs were calculated using the approach outlined in the EU Technical Guidance for Risk
Assessment of New and Existing Chemicals, assuming, where appropriate, initial on-site STP
treatment followed by release to a municipal STP or surface water. Local PEC values calculated
for the aquatic compartment and for air for individual production and processing facilities are
reproduced in the Appendix.
The following results were obtained for regional and continental PECs for water and air:
PECregionalwater
2.81 µg/l
PECcontinentalwater
0.41 µg/l
PECregionalair
7.08.10-5 mg/m3
PECcontinentalair
2.49.10-5 mg/m3
Monitoring data indicate that concentrations of acrylonitrile in surface waters are generally
below the limit of detection of 1-2 µg/l. In relation to measured levels of acrylonitrile in air, a
study of acrylonitrile in urban German air over the period 1977–1984 indicated levels of
between 0.01-10.4 µg/m3, while clean (rural) air contained less than 0.002 µg/m3.
Acrylonitrile was not detected over a 6-month monitoring period of urbanised and
industrialised air in the Gulf Coast of Texas (limit of detection 0.122 µg/m3).
In relation to the terrestrial compartment, the PEClocalsoil was calculated assuming sludge
from a WWTP containing acrylonitrile was applied to soil once a year for 10 years, to which
was added the contribution loads from wet and dry deposition. The result for PEClocalsoil for
processing sites was 3.86 µg/kg wet weight (wwt) averaged over 30 days or 180 days. The
value for production was 0.17 mg/kg wet weight averaged over 30 days or 0.046 mg/kg wet
weight averaged 180 days, while PEClocal in soil pore water (agricultural soil) was
0.3 mg/kg wwt. It should be noted, however, that this is a worst-case exposure scenario, and
appears unrealistic, given the information from industry that little industrial sludge from
acrylonitrile production and processing facilities is spread on land in Europe. The majority of
companies providing information on this aspect indicated that contaminated sludge is
incinerated together with other wastes. The conclusion however cannot be extrapolated to
sites not covered by this risk assessment. Given the very low levels of acrylonitrile anticipated
to be present in the terrestrial environment, no significant levels are expected in plants or
other terrestrial species, potential routes of exposure being deposition from air or
contaminated effluents or surface waters.
EUSES provides values for exposed biota, as follows:
Regional concentration in wet fish, mg/kg:
Regional concentration in plant root tissue, mg/kg:
Regional concentration in plant leaves, mg/kg:
Regional concentration in grass, mg/kg:
Regional concentration in meat (wet weight), mg/kg:
Regional concentration in milk (wet weight), mg/kg:
7
3.96.10-3
1.3.10-4
1.66.10-5
1.66.10-5
1.30.10-7
1.30.10-6
EU RISK ASSESSMENT - ACRYLONITRILE
SUMMARY, 2004
EUSES also provides values for daily human intake from the environment, as follows:
Daily intake through drinking water (mg/kg/day):
Daily intake through consumption of fish (mg/kg/day):
Daily intake through consumption of leaf crops (mg/kg/day):
Daily intake through consumption of root crops (mg/kg/day):
Daily intake through consumption of meat (mg/kg/day):
Daily intake through consumption of milk (mg/kg/day):
Daily intake through intake of air (mg/kg/day):
Regional total daily intake for humans (mg/kg/day)
8.01.10-5
6.51.10-6
2.84.10-7
7.12.10-7
5.61.10-10
1.04.10-8
1.52.10-5
1.03.10-4
It is concluded from these results that the potential for secondary poisoning is very small.
3.2
EFFECTS ASSESSMENT
Acrylonitrile is toxic to aquatic organisms. Valid short-term L(E)C50s for acrylonitrile have
been reported for fish, Daphnia, algae and microorganisms. The most reliable result in fish is
considered to be that in the saltwater species Cyprinodon variegatus in which a 96-hour LC50
of 8.6 mg/l was reported. The absolute validity of the lower figure of 5.2 mg/l for
Ctenophayngodon idellus cannot be ascertained. The lowest 48-hour EC50 for Daphnia was
7.6 mg/l (nominal concentration, Daphnia magna). Two valid results are available for the
72-hour EC50 (biomass) in algae, 2.5 mg/l in Scenedesmus subspicatus and 1.63 mg/l
(measured concentration at t0) in the saltwater diatom Skeletonema costatum.
Long-term toxicity data are available in fish, Daphnia and algae. The fish early life stage
toxicity test in Pimephales promelas, using flow-through conditions, provided a
LOEC/NOEC of 0.34 mg/l, while a 30-day flow through test in mature fish of the same
species provided a long-term LC50 of 2.6 mg/l. If the value of 0.34 mg/l is taken as a LOEC, a
NOEC may be derived by application of a safety factor of 2, giving a NOEC of 0.17 mg/l.
The 14/21-day life cycle study in Daphnia magna provided a NOEC of 0.5 mg/l (nominal),
while NOECs for effects on biomass in algae are reported as 0.8 mg/l (Scenedesmus
subspicatus) and 0.41 mg/l (Skeletonema costatum). For risk characterisation purposes, a
PNEC has been derived using an assessment factor of 10. Applying this factor to the NOEC
derived from the fish early life stage toxicity test in Pimephales promelas gives a PNEC of
17 µg/l.
The results of microbial toxicity tests and biodegradation studies on acrylonitrile indicate a
potential effect on microorganisms in wastewater treatment plants, at least on start-up. The
reported EC50s range from 1 - > 1,800 mg/l. Results with acclimated microbial populations
and in simulation tests have indicated no inhibitory effect of acrylonitrile at levels as high as
200 mg/l, and a conservative estimate of 50 mg/l for a NOEC in such populations has been
assumed. Application of a factor of 10 to this NOEC derives a PNEC of 5 mg/l for
microorganisms in acclimated wastewater treatment plants handling acrylonitrile on a
continuous basis. A factor of 10 is considered justified given the relatively large body of data
on microbial toxicity of acrylonitrile.
PECsediment and PNECsediment can be derived from the results for water. A PNEC for sediment
of 0.0126 mg/kg (based on PNEC (aquatic) of 17 µg/l) was derived using the above approach.
A PNEC for soil of 0.00268 mg/kg was derived, based on PNEC (aquatic) of 17 µg/l. The
reported NOEC for soil microorganisms is comparatively high, at approximately 100 mg/kg,
providing a PNEC of 100 µg/kg (assessment factor 1,000). Data available for derivation of a
8
CHAPTER 3. ENVIRONMENT
PNEC for non-soil-dwelling terrestrial organisms are limited and of unknown quality. Using
the LC50 data generated in a number of insect species and assuming a conservative figure of
0.5 mg/l for the LC50 gives a PNEC of 0.5 µg/l air
3.3
RISK CHARACTERISATION
Acrylonitrile is toxic to aquatic organisms and is not readily biodegradable. Release into the
aquatic environment could therefore possibly present some risk to aquatic species in the
vicinity of plants producing or further processing acrylonitrile. Information from simulation
tests and on the performance of wastewater biotreatment plants in a number of companies
indicates that greater than 90% biodegradation is achieved in acclimated WWTPs. Of the
43 companies producing or processing acrylonitrile in the European Union, 33 have dedicated
industrial WWTPs and a further 2 discharge to municipal WWTP. The PEC:PNEC ratio for
the aquatic compartment (water and sediment) for all but 1 of these 43 companies is below
1.0, indicating that the risk is adequately managed by the control measures in place. In the
case of one site, located on a large marine estuary, application of a specific dilution factor of
701 derived from modelling of the dilution due to seawater results in a PEC:PNEC ratio of
3.1 for water and 3.46 for sediment. It is concluded that there are concerns for possible effects
on the local aquatic environmental sphere as a consequence of exposure arising from
production of acrylic fibres at this site only.3 It should be noted, however, that this conclusion
applies only at a particular point in time to 42 out of the total of 43 European sites existing at
the time and which provided aquatic release data relating to the period 1994-1996, and cannot
be extrapolated generally for the aquatic environment. The specific risk reduction measures
(eg wastewater treatment) or particular characteristics of the assessed sites (e.g. high dilution
factors due to effluent emissions into very large rivers or estuaries) cannot be extrapolated to
sites not covered by this risk assessment, for example new sites starting up after the data for
this assessment were gathered, or sites located outside the European Union.
In relation to risk assessment for microorganisms in wastewater treatment plants, a PNEC of
5 mg/l is estimated for sites with acclimatised WWTPs, while for non-acclimated WWTPS a
PNEC of 100 µg/l was derived. For sites with WWTP which produced measured data for
effluent, concentrations ranged from 0 to 5.8 mg/l. Appendices A and B show that the
PEC:PNEC ratios for sites having WWTP are all below 1.0. It can be concluded that there is
little or no risk for microorganisms in industrial WWTP, although some risk may exist in nonacclimated WWTP. In practice the companies providing data for this report have indicated
that, in the main, their WWTPs operate continually and are fully acclimatised to acrylonitrile
waste.
3
Since the publication of the risk assessment, the site in question has participated with the relevant national
authority in working on a risk reduction programme. The aim of the programme was to first quantify the risk by
measuring actual acrylonitrile in the receiving waters. A modelling and sampling exercise took place in 2000
using a team of independent consultants approved by the Authorities. The position of the effluent plume was
determined using a number of techniques including dye tracing, drogue tracking and analysis of species known
to be present in the effluent. Effluent samples were taken in the effluent plume on two separate occasions at
distances between 100 and 5,000 m from the effluent discharge pipe. The level of acrylonitrile present in all
samples was below the analytical detection limit of 1.3 µg/l and therefore well below the PNEC of 17 µg/l. The
most plausible explanation for the results to date is that acrylonitrile in the effluent is being degraded rapidly by
bacteria that have become acclimatised to using acrylonitrile as a food source. Sediment samples taken during
the survey proved that the benthic fauna composition was as expected and healthy. At a meeting with the
authorities, it was agreed that a future work programme might include another survey to determine if changes to
the make up of the production units on the site have made any difference to the results.
9
EU RISK ASSESSMENT - ACRYLONITRILE
SUMMARY, 2004
Although the atmospheric compartment is the major compartment of distribution of
acrylonitrile, there is rapid photodegradation (t1/2 approximately 5 days). Local emissions
from production and processing facilities can be predicted to give rise to the highest
atmospheric concentrations, and the calculated PEClocalair for sites providing specific
emission data lies between 0 and 0.240 mg/m3 or 1-240 µg/l. Results of monitoring at the
perimeter of acrylonitrile plants shows that levels are generally below 1 µg/m3. No effect
information is available, other than the effects of acrylonitrile on a number of insect species
known to infest food, which showed an LC50 of 0.5 mg/l, and therefore a PNEC of 0.5 µg/l.
However the quality of these studies is questionable, and also taking into account the
measured levels in the vicinity of plants it is concluded that there is little risk associated with
exposure of ecosystems to atmospheric environmental levels of acrylonitrile. The PEC:PNEC
ratios for air are all below 1.0.
In relation to the terrestrial compartment, the estimate of PECregionalsoil reflects primarily
point source emissions from production or further processing, and diffuse emissions from car
exhausts etc. have not been taken into account in the EUSES input. However, even with a
significant contribution to PECregionalsoil from such sources, the PEC:PNEC ratio will still be
well below 1, again indicating little concern for this compartment.
10
4
HUMAN HEALTH
4.1
HUMAN HEALTH (TOXICITY)
4.1.1
Exposure assessment
The human population may be exposed to acrylonitrile at the workplace, and to a
minimal/negligible extent indirectly via the environment. Exposure of consumers is also
possible, via use or wearing of materials which may contain a small percentage of unreacted
acrylonitrile monomer, or via food which is packaged in containers made from acrylonitrilederived plastics.
Occupational exposure
Acrylonitrile is released during industrial production and processing to air and wastewater.
The main human exposure is via air (inhalation) regarding occupationally exposed workers.
As acrylonitrile is produced and almost totally processed in a closed system, the main concern
relating to exposure relates to the accident scenario or due to breaches in the closed system.
The 8-hour time-weighted average Occupational Exposure Limit in the majority of countries
having such a limit is between 2 and 3 ppm. Only 3 countries list short-term exposure limits
(STELs), of 5, 6, and 0.23 ppm (11.25, 13.5 and 0.5 mg/m3), respectively the last coming
from the former USSR.
The exposure assessment was based on measured data, expert judgement, on-site experience,
and the EASE model (inhalation and dermal exposure assessment). Measured data on
exposure levels for acrylonitrile in the mid-1970s indicated average levels of as high as
5 ppm. By the late 1980s and early 1990s, exposure levels were in the range of < 0.12 ppm to
0.49 ppm (8-h time-weighted average values, personal monitoring). Monitoring from the mid1990s onwards indicates that average exposure levels throughout Europe for processing and
production of acrylonitrile were 0.1 ppm and 0.45 ppm, respectively. Industry has confirmed
that current exposure levels are significantly lower than those in earlier decades, reflecting
improvements in workplace exposure control over the last decade. However for the purpose
of risk characterisation a reasonable worst-case exposure level of 2 ppm (the 8-hour
Occupational Exposure Limit in a number of countries) has been used for both production and
further processing.
Dermal exposure to acrylonitrile during production is considered to be very unlikely under
normal conditions of work as closed systems are used. Dermal exposure of workers was
however considered in the risk assessment during processing of acrylonitrile to polymers
including fibre production, where direct handling/contact could possibly occur. In practice,
industry has confirmed that exposure by the dermal route does not occur, due to stringent use
of personal protective equipment. Nevertheless, for dermal exposure a worst-case scenario
was assumed i.e. between 0.0 and 0.1 mg/cm2/day, based on EASE Modelling predictions.
The concentration of acrylonitrile in end-use products is low. Therefore, airborne exposure or
dermal exposure of workers during the handling of such products will be minimal. Measured
data indicate that levels of acrylonitrile in this situation are below the level of detection.
11
EU RISK ASSESSMENT - ACRYLONITRILE
SUMMARY, 2004
Consumer exposure
Acrylonitrile is not sold to the general public alone or as part of a preparation. Based on the
identified uses in products, the main routes for potential exposure of consumers are via dermal
contact/absorption through the skin, due to slow release of acrylonitrile from acrylic fibres in
clothes, and via consumption/ingestion of foods packaged in acrylonitrile-derived plastics and
migration of residual acrylonitrile monomer from the food packaging into food.
Residual low levels of acrylonitrile have been reported in a number of commercial polymeric
materials derived from acrylonitrile. For fibres, reported levels were generally less than
1 mg/kg (1 ppm), and recent work carried out by industry indicate that current levels in both
acrylic fibres and in garments derived from them are well below 1 ppm. In the risk
assessment, possible migration of residual acrylonitrile from fibres was estimated with the
AMEM-programme (OECD, 1993). The results indicated little potential for exposure of
consumers to residual monomer in this situation. Based on the comprehensive work carried
out by one major fibre producer it can be concluded that current and foreseeable users of
products containing acrylonitrile-based fibres are at negligible risk from exposure to residual
acrylonitrile content.
The tolerable specific migration limit is 0.02 mg acrylonitrile / kg food for food products
contained in ABS plastic, as laid down by Commission Directive 90/128/EEC. If it is
assumed that only 5% of human food is packaged in ABS and an average person consumes
2 kg of food and beverages/day, human intake will be no more than 2 µg/day or
0.03 µg/kg/day in the case of a bodyweight of 70 kg.
Humans exposed via the environment
Exposure of the general public via the environment is considered at two levels: (1) exposure
to background levels on a regional or continental basis, and (2) exposure to potentially higher
levels which may exist near industrial production and processing sites. The compartments
considered for both cases are biota, drinking water and air. With respect to the regional
exposure predicted results from the Mackay Level 3 model were far below those estimates
calculated using EUSES. The EUSES value for Regional total daily intake for humans is
calculated as 1.03.10-4 mg/kg/day. Actual monitoring data indicate that levels of acrylonitrile
are below the limits of detection in both air and drinking water, while no data were found for
levels of acrylonitrile in biota.
Regarding the local case (2) the emissions data from European industry indicate that predicted
local concentrations in water courses in the immediate vicinity of inland sites for production
and processing of acrylonitrile range from 0-6 µg/l (background regional levels of 3 µg/l are
predicted from EUSES). Higher levels were predicted in the vicinity of coastal sites without
WWTP, discharging directly into the sea. However, given the continuing degradation of
acrylonitrile, which is predicted to occur following initial release to local surface water and
the lack of bioaccumulation potential, it is anticipated that levels of acrylonitrile in local biota
will be extremely low. The assumption was made that these levels will be similar to those
predicted on a regional scale by EUSES. Therefore it can be concluded that people living
close to or in the vicinity of acrylonitrile production or processing plants are exposed to low
to negligible levels of acrylonitrile in the air.
12
CHAPTER 4. HUMAN HEALTH
4.1.2
Effects assessment
Based on the results of animal studies and available human evidence, acute effects of
acrylonitrile can occur following inhalation, ingestion and dermal exposure. Clinical signs
resulting from acrylonitrile have been examined in a number of different animal species and
have been found to vary very little between species.
Only limited data exist (specific accidents or incidents) with respect to exposure of humans.
However these findings and dose levels are consistent with the information obtained from
acute studies performed in animals. Based therefore mainly on the animal data, acrylonitrile is
toxic by the oral, dermal and inhalation routes and causes neurotoxic effects (which relate
both to acrylonitrile itself and also to the release of cyanide). Acrylonitrile should therefore be
classified as “Toxic by inhalation, in contact with skin and if swallowed” (for classification,
see Section 1).
Acrylonitrile is irritating to the skin and is a severe eye irritant. While there are no specific
animal studies on respiratory irritancy, both short-term and long-term studies in a range of
species have indicated that acrylonitrile produces irritant effects on the upper respiratory tract.
As such therefore acrylonitrile should be classified as “Irritant, irritating to respiratory system
and skin, risk of serious damage to eyes” (see Section 1).
Acrylonitrile is a skin sensitiser and should be classified as “Sensitising, May cause
sensitisation by skin contact” (see Section 1). While there is no available data with respect to
respiratory sensitisation, in practice, there are no reports of respiratory sensitisation in
exposed workers. In addition, it is recognised that the control measures that have been in
place for many years to protect workers against the carcinogenic effects of acrylonitrile will
also protect against possible induction of sensitisation.
Studies on the toxicokinetics of acrylonitrile have shown that it is extensively absorbed and
distributed after all routes of administration. Limited toxicokinetics data in humans indicate
that the metabolic pathway via cyanoethylene oxide (CEO) exists in humans and generally
support the conclusion that the metabolic pathways observed in experimental animals are also
operative in humans. However there is further evidence that humans may possess an
additional detoxification pathway, epoxide hyrolase, for CEO, which should decrease the
amount of CEO leaving the liver to the systemic circulation relative to rats, where this
pathway is not operative.
A large number of long-term toxicity/ carcinogenicity studies have been carried out on
acrylonitrile, using the oral and inhalation routes. Both routes of exposure have been
associated with lethality in a range of animal species. Target organs have been the kidney,
gastrointestinal tract, central nervous system and adrenals. Neurotoxicological effects can
largely be explained on the basis of release of cyanide, which may also be the ultimate
causative agent in relation to the repeat dose toxicity of acrylonitrile. Local irritant effects
have been observed in the respiratory tract following inhalation exposure. Human data are
difficult to assess in relation to establishment of a dose-response relationship for chronic
toxicity. However many of the findings in the animal repeat dose exposure studies, especially
the neurological and irritation effects, reflected the reported findings in workers.
The most relevant long term toxicity/carcinogenicity study with respect to the oral route of
exposure was performed by Biodynamics, in which acrylonitrile was administered orally via
drinking water to 100 Fisher 344 rats/sex/group at dose levels of 1, 3, 10, 30, and 100 ppm
and to a control group of 200 rats/sex. Treatment-related non-neoplastic changes were seen at
10 ppm and upwards. Mortality was increased in males at 10 ppm and in females an increase
13
EU RISK ASSESSMENT - ACRYLONITRILE
SUMMARY, 2004
was observed at 3 and 30 ppm. However the increase at 3 ppm was small and did not indicate
a dose-response relationship. The first true indication of a dose-response relationship for
mortality in females began at the 10 ppm dose level. This study was used to establish an
NO(A)EL of 3 ppm (equivalent to an average daily dose of 0.25 mg/kg/day in males and
0.36 mg/kg/day in females) for the oral (drinking water) route of exposure.
In relation to the inhalation route, the Quast et al. carcinogenicity study was considered to be
the key study for risk assessment purposes. Non-neoplastic changes observed in SpragueDawley rats exposed to 20 ppm or 80 ppm acrylonitrile for 6 hours/day, 5days/week, for
104 weeks, compromised growth retardation and early mortality in both sexes at 80 ppm and
in females at 20 ppm. As a result of irritation due to acrylonitrile exposure, inflammatory and
degenerative changes (hyperplasia and metaplasia of the respiratory epithelium) were present
in the nasal turbinates of both exposed groups (20 and 80 ppm). A significantly increased
number of rats in the 80 ppm exposure group also showed focal gliosis and perivascular
cuffing in the brain. From the effects seen in this study it was concluded that the NO(A)EL is
less than 20 ppm (lowest dose administered). This value of 20 ppm was considered the
LO(A)EL, based on the nasal changes (local effect) which were evident at this concentration.
Application of a safety factor of 5 to the level of 20 ppm to give a suggested No Adverse
Effect level (NAEL) of 4 ppm was considered justifiable because of the nature of the effect
(local irritancy) and the conclusion that other systemic, non-neoplastic findings in
acrylonitrile-treated rats were secondary to its tumorigenic effects, rather than due to direct
systemic toxicity. The conclusion is supported by the evidence from the study of Sakurai et al.
(1978) that levels below 10 ppm (22.5 mg/m3) did not cause notable irritancy.
The results of the long-term toxicity/ carcinogenicity studies indicate conclusively that
acrylonitrile is carcinogenic via both the oral and inhalation routes. The animals developed
tumours of the central nervous system, forestomach, intestines (including gastrointestinal
tract, tongue, non-glandular stomach and small intestine), Zymbal gland (a sebaceous tissue
associated with the ear duct of rodent species) and the mammary glands. While there is no
doubt that acrylonitrile is an animal carcinogen the mechanism of action with respect to
carcinogenicity is still relatively unclear. However as there is no definitive contrary evidence
acrylonitrile must be considered to be a genotoxic carcinogen and as such it is not possible to
establish a safe threshold regarding exposure to the substance. On this basis a NOEL cannot
in practice be estimated or established for this particular end-point.
Acrylonitrile is weakly mutagenic in reverse mutation assays, the effect generally requiring
the presence of metabolic activation. Positive results have also been obtained in mutagenicity
assays using yeast and Aspergillus and in mammalian cell lines including mouse lymphoma
cells (TK+/- locus and oua locus) and the TK6 human lymphoblast cell line. These again
generally required metabolic activation (frequently only at cytotoxic concentrations).
Acrylonitrile induces sister chromatid exchanges and chromosomal aberrations in in vitro
studies, however negative responses have generally been obtained in DNA repair assays using
rat hepatocytes and human epithelial cells in vitro. In in vivo studies overall acrylonitrile
appeared to be negative in a dominant lethal assay in rats, and was also negative in two mouse
micronucleus studies. Conflicting results have been obtained in studies of unscheduled DNA
synthesis. A number of studies in Drosophila, using a range of genetic markers, have given
positive results.
Overall, although acrylonitrile has been shown to be weakly mutagenic in in vitro systems,
indicative of genotoxic potential, these findings are not reliably reflected in the in vivo
situation. This suggests that acrylonitrile or its active metabolites do not reach target tissues in
vivo, possibly due to the detoxification of the epoxide metabolite CEO via a glutathione
14
CHAPTER 4. HUMAN HEALTH
conjugation pathway which may not exist in in vitro test systems. Nevertheless, the body of
evidence presented in this report (in vitro), together with the positive results in Drosophila,
leads to the conclusion that acrylonitrile must be regarded as genotoxic.
A vast amount of epidemiological data exists and various meta-analyses have considered this
information. In summary, the excess risk of lung cancer from acrylonitrile exposure, if any, is
small. For the less common cancers such as brain and prostate it is only possible to evaluate
consistency across the available studies. When doing this a relatively imprecise estimate of
risk was found for prostate and brain cancers. On the basis of the most recent studies
however, there is little or no evidence to support a causal relationship between acrylonitrile
exposure and cancer in man. From the results of the animals studies acrylonitrile is an animal
carcinogen and the current classification as a Category 2 carcinogen is appropriate (see
Section 1). However based on the evidence presented, in particular the epidemiological
information available, while acrylonitrile is an animal carcinogen the risk to humans is low
considering current exposure in the workplace and the lack of association arising from the
large cohort studies performed.
The results of a 3-generation reproduction study did not show any effects on fertility,
although effects were seen on pup viability and bodyweights of pups in all 3 generations at
21 days were also reduced. These effects could be attributed to maternal toxicity. A number of
other studies have also indicated that acrylonitrile is foetoxic, as evidenced by dose-dependent
reductions in pup weight at exposure levels which are also maternally toxic. A No Effect
Level of 12 ppm for the foetotoxic effect was established. While effects on the testis in mice
and rats have been reported by some authors in short term studies, this may have been a
secondary effect associated with systemic toxicity. However, testicular toxicity has not been
reported in a 2-year inhalation study in rats at 80 ppm (equivalent oral uptake 17 mg/kg/day)
or in a 90-day oral gavage study in mice at a top dose of 12 mg/kg/day. There are no data on
fertility in humans.
It can be concluded that existing animal data do not show any clear indication of fertility,
dominant lethal, reproductive or teratogenic effects of acrylonitrile at doses below those
producing parental toxicity. Classification as toxic for reproduction is not considered
appropriate given the maternal toxicity seen, the confounding influence of disease and the
negative outcome of the 1993 developmental study where previously mated rats were exposed
to dose levels of 0, 12, 25, 50 and 100 ppm acrylonitrile by inhalation 6 hr/day from day 6-20
of gestation.
4.1.3
Risk characterisation
Workers
Exposure of humans to acrylonitrile is possible in the workplace, during production of
acrylonitrile and its use in the manufacture of acrylic fibres, ABS-SAN plastics, nitrile
rubbers, other intermediates such as acrylamide and adiponitrile and other end uses.
Conclusion (iii) is reached in relation to the following end points: (1) repeated dose
(systemic) toxicity, (2) carcinogenicity.
In relation to conclusion (iii) for repeated dose (systemic) toxicity by the inhalation and by
route-to-route extrapolation, the dermal route, this primarily reflects the toxicity seen in
15
EU RISK ASSESSMENT - ACRYLONITRILE
SUMMARY, 2004
chronic studies in rats and the relatively low Margins of Safety (MOSs) between anticipated
exposure levels and doses producing toxicity. Many of the findings in the animal repeated
dose studies are mirrored in reported findings in workers. Overall, however, the human data
are difficult to assess in relation to establishment of a dose-response relationship. The EU
Working Group on Classification and Labelling agreed that acrylonitrile should not be
classified with R 48 (risk of serious damage to health on prolonged exposure) based on the
information available. Nevertheless, for the purposes of this risk assessment, given the
difficulties in assessing the human data and the low MOSs achieved, it is recommended that
conclusion (iii) be applied to the repeated dose (systemic) toxicity end point. It is however
acknowledged that strict controls on exposure to acrylonitrile apply in the industry for this
classified carcinogen, and industry confirm that exposure levels in the workplace are much
less than 2 ppm. For example in the 1990s, in production and processing sectors, the levels
achieved were less than 1 ppm and 0.1-1 ppm, respectively.
In relation to conclusion (iii) for carcinogenicity, it is accepted that there is a risk at any level
of exposure, given that acrylonitrile is currently regarded as a carcinogen for which a
threshold cannot be reliably identified. The magnitude of this risk has been estimated to lie
between 1.3.10-4 to 1.8.10-2 for workers exposed to 2 ppm (the current OEL in a number of
EU countries) for 8 hours a day, 5 days a week and a working life of 40 years. A Margin of
Exposure (MOE) of 57.5 has been derived, based on a T25 of 16.1 mg/kg/day in the male rat
obtained from the Quast 2-year inhalation study.
Conclusion (ii) is reached for the end points of acute toxicity, skin, eye and respiratory
irritancy, skin sensitisation, corrosivity, repeated dose (local) toxicity by the inhalation route,
neurotoxicity, mutagenicity and reproductive toxicity.
Consumers
There is no exposure of consumers directly to acrylonitrile. However there is potential for
indirect exposure of consumers as a consequence of use of products manufactured from
acrylonitrile, due to the presence of residual monomer. Risk characterisation for the endpoints
of acute toxicity, irritation and corrosivity is not necessary given that consumers will never
come in contact with acrylonitrile liquid. The relevant endpoints therefore are skin
sensitisation, repeat dose toxicity, carcinogenicity, mutagenicity and reproductive toxicity.
Conclusion (iii) is reached for the end point carcinogenicity.
Regarding the level of carcinogenic risk for consumers related to inhalation of acrylonitrile, a
life time exposure scenario where a 70 kg man inhales 20 m3 of air a day, containing 1 part
per trillion acrylonitrile a risk estimate of 3.3.10-8 was derived. More recently this database
was re-evaluated using the EPA’s cancer risk assessment guidelines giving a risk estimate of
between 8.2.10-6 to 1.1.10-5 associated with lifetime continuous exposure to 1 µg/m3
(0.44.10-3 ppm). In addition the Committee on Carcinogenicity of Chemicals in Food (UK)
and the Food Additives and Contamination Committee (UK) considered the levels of
contamination with acrylonitrile monomer to be very low and that the general public were not
at a measurable risk from exposure to acrylonitrile.
However, acrylonitrile is a carcinogen for which a threshold cannot be reliably identified;
therefore it is considered that conclusion (iii) is appropriate, since risks cannot be excluded
for all exposure scenarios. However, since the predicted exposures are very low, the risks will
16
CHAPTER 4. HUMAN HEALTH
be already very low, and this should be taken into account when considering the adequacy of
controls feasibility and practicability of further specific risk reduction measures.
Conclusion (ii) is reached for the end points of skin sensitisation, repeated dose toxicity by
the inhalation or (by route-to-route extrapolation) the dermal route, mutagenicity and
reproductive toxicity, based on the calculated reasonable worst-case exposure levels and the
margins of safety achieved.
Humans exposed via the environment
Indirect exposure of the general public via the environment from consumption of biota or
drinking water and exposure to air containing residual acrylonitrile is theoretically possible
although considered to be of low risk due to the extremely low levels calculated or derived
from actual monitoring data. Assessment of exposure via this route identified two populations
for consideration i.e. (1) populations exposed to background levels on a regional or
continental basis and (2) populations exposed to potentially higher levels which could
conceivably be found near industrial production and processing sites.
While acrylonitrile is acutely toxic, irritant and sensitising, it is considered that there is no
concern for populations in either category (1) or category (2) in relation to these hazards, by
any route of exposure, given the very low levels of exposure anticipated: conclusion (ii).
In relation to mutagenicity, reflecting the absence of in vivo mutagenicity, the rapid
detoxification of the mutagenic metabolite CEO in human by epoxide hydrolase and the fact that
acrylonitrile is not classified as mutagenic, acrylonitrile is of no concern for this end point:
conclusion (ii).
The endpoint of concern remaining is carcinogenicity. There could be some concern for
carcinogenicity for humans exposed via air, with respect to the immediate vicinity of plants
(conclusion (iii)), based mainly on potential for local exposure to a carcinogen for which a
threshold cannot be reliably identified. This conclusion however should be qualified
indicating that risks are already very low. This should be taken into account when considering
the adequacy of controls feasibility and practicability of further specific risk reduction
measures.
4.2
HUMAN HEALTH (PHYSICO-CHEMICAL PROPERTIES)
Assessment of physico-chemical hazards has indicated that acrylonitrile is highly flammable
and has explosive properties when mixed with air in certain proportions. Spontaneous
exothermic polymerisation of acrylonitrile also presents a risk of explosion. The use of closed
systems and stringent safety controls indicates that the potential risk to workers is minimal
under conditions of normal handling and use: conclusion (ii).
In relation to consumers, given the very low levels of free (un-reacted) monomer to which
they are likely to be exposed, it is concluded that acrylonitrile is unlikely to present a risk to
this population due to physico-chemical hazards: conclusion (ii).
17
5
RESULTS
5.1
ENVIRONMENT
Aquatic compartment (incl. sediment)
Conclusion (iii)
There is a need for limiting the risks; risk reduction measures which are
already being applied shall be taken into account.
This conclusion is reached because of concerns for effects on the local aquatic sphere (including
sediment) as a consequence of exposure arising from production of acrylic fibres at a particular
site.
Conclusion (ii)
There is at present no need for further information or testing or risk reduction
measures beyond those which are being applied already.
This conclusion applies to the aquatic compartment including sediment and microorganisms, for
production of acrylonitrile and further processing to fibres and other plastics, with the exception
of processing to acrylic fibres at one site only.
It also applies to the terrestrial compartment, atmospheric compartment and secondary
poisoning, for production of acrylonitrile and further processing to fibres and other plastics.
5.2
HUMAN HEALTH
5.2.1
Human health (toxicity)
Workers
Conclusion (iii)
There is a need for limiting the risks; risk reduction measures which are
already being applied shall be taken into account.
This conclusion is reached because of concerns for general systemic effects and carcinogenicity
as a consequence of exposure arising during the production and processing of the substance.
Conclusion (ii)
There is at present no need for further information or testing or risk reduction
measures beyond those which are being applied already.
This conclusion applies to the end points of acute toxicity, skin, eye and respiratory irritancy,
skin sensitisation, corrosivity, repeated dose (local) toxicity by the inhalation route,
neurotoxicity, mutagenicity and reproductive toxicity.
Consumers
Conclusion (iii)
There is a need for limiting the risks; risk reduction measures which are
already being applied shall be taken into account.
This conclusion is reached because of concerns for carcinogenicity.
Risks cannot be excluded for all exposure scenarios, as the substance is identified as a nonthreshold carcinogen. The adequacy of existing controls and the feasibility and practicability of
18
CHAPTER 5. RESULTS
further specific measures should be considered. However, the risk assessment indicates that risks
are already low. This should be taken into account when considering the adequacy of existing
controls and the feasibility and practicability of further specific risk reduction measures.
Conclusion (ii)
There is at present no need for further information or testing or risk reduction
measures beyond those which are being applied already.
This conclusion applies to the end points of skin sensitisation, repeated dose toxicity by the
inhalation or (by route-to-route extrapolation) the dermal route, mutagenicity and reproductive
toxicity.
Humans exposed via the environment
Conclusion (iii)
There is a need for limiting the risks; risk reduction measures which are
already being applied shall be taken into account.
This conclusion is reached because of concerns for carcinogenicity after highest predicted
atmosphere concentrations at a local level.
There could be some concern for carcinogenicity for humans exposed via air, with respect to the
immediate vicinity of plants, based mainly on potential for local exposure to a carcinogen for
which a threshold cannot be reliably identified. This conclusion however should be qualified
indicating that risks are already very low. This should be taken into account when considering
the adequacy of controls feasibility and practicability of further specific risk reduction measures.
Conclusion (ii)
There is at present no need for further information or testing or risk reduction
measures beyond those which are being applied already.
This conclusion applies to all other endpoints.
5.2.2
Human health (risks from physico-chemical properties)
Conclusion (ii)
There is at present no need for further information and/or testing or for risk
reduction measures beyond those which are being applied already.
This conclusion is reached because the risk assessment shows that risks to workers, consumers
and humans exposed via the environment related to physico-chemical properties are not
expected. Risk reduction measures already being applied are considered sufficient.
19
Appendix A Local PEC and other emission parameters for surface water for acrylonitrile production
plants in Europe
Table A.1 Local PEC and other emission parameters for surface water for acrylonitrile production plants in Europe
In this and subsequent PEC tables, some values are based on detection limits. Thus their PEC is a 'less than' value.
Site
Production Released Daily release
C, influent C effluent Discharge
t/y
t/y
t/d
WWTP
mg/l
mg/l *
to
1
0.0003
Yes
0.167
0.1000
sea
120500
0.100
2 (+BB)
0.0133
Yes
190000
4.000
3.800
0.0013
river
3
0.0001
Yes
0.0036
85000
0.043
2.500
sea
4 (+D+EE) 300000
0.0001
Yes
0.052
0.031
0.0020
river
5
0.0310
No
15.500
280000
9.300
5.8000 estuary
6
0.0001
Yes
0.067
60000
0.040
0.3700
river
7
0.0001
Yes
0.040
110000
0.024
0.0500
river
8
0.0002
Yes
0.0044
105000
0.053
2.500
sea
Total
1250500
13.59
Note
Dilution C, water
C water an PEC, waterPEC wat.an
factor
mg/l
mg/l
mg/l
mg/l
10 0.010000 0.00822
0.0128
0.0110
0.0029
0.0028
30 0.000043 0.00004
10 0.000363 0.00030
0.0032
0.0031
0.0028
0.0028
1529 0.000001 0.00000
0.0144
0.0123
500 0.011600 0.00953
0.0030
0.0030
2000 0.000185 0.00015
0.0028
0.0028
4154 0.000012 0.00001
10 0.000439 0.00036
0.0032
0.0032
RCR PEC, sed
water
mg/kg
0.754 0.01058
0.168 0.00236
0.187 0.00262
0.165 0.00232
0.848 0.01190
0.176 0.00247
0.166 0.00233
0.191 0.00268
RCRstp RCR sed
0.0200
0.0003
0.0007
0.0004
n.a.
0.0740
0.0100
0.0009
21
APPENDIX A
Numbers in bold italics actual figures
Where a production facility and further processing facility(s) are located at the same site, the production figure in column 2
is for the production site only, but emissions relate to all facilities at the site (as in 4 (+D+EE)
Production figures rounded to nearest 100.
Where an influent concentration was lower than an effluent concentration calculated, the influent was used as the effluent concentration
p.a.release / 300 = daily release t/d
[Daily release (t/d) / STP volume (default 2,000,000 l/d)] x 1,000,000,000 (convert t to mg) = C, influent mg/l
C, effluent = C, influent * fraction to water (EUSES 0.116). This accounts for fraction of 0.85 being degraded, 0.0324 discharged to air, and a fraction of 0.00132 in sludge.
Note that the fraction effluent degraded in STP of 0.885 is from EUSES for readily biodegradable, as agreed for industrial sites with WWTP, but does not apply to site 5
However, it was only necessary to apply these fractions for sites which had not provided effluent concentrations.
For sites 3 and 8, C, effluent = C, influent/80*0.116 and C, influent/66*0.116 respectively, since the acrylonitrile waste stream is further diluted
by other aqueous waste (240 m3 in 19.200 m3 and 360 m3 in 24,000 m3 respectively ) before discharge into WWTP
C, effluent / dilution factor (default 10) = C, water.
Where a site discharges to an estuary the dilution factor has been derived from the main river flow into the estuary only.
Where additional dilution data has been available for WWTP this has been used in calculating effluent concentrations.
C water + PEC regional = PEC water (PEC regional (EUSES) = 0.00281)
PEC water, annual = C, water annual + PEC regional (PEC regional (EUSES) = 0.00281)
C water * 300/365 = C, water annual
RCR = PEC/PNEC
PNEC surfacewater = 0.017 where NOEC / 10
* C local effluent = PEC STP
RCR stp = PEC stp / PNEC where PNEC = 5 mg/l
PEC sediment = (0.95/1150)*1000*PECwater = 0.8260869 * PECwater
PNEC sediment = 0.0126 mg/kg (Section 3.2.1.4)
0.8399
0.1871
0.2080
0.1843
0.9448
0.1964
0.1850
0.2130
Appendix B Local PEC and other emission parameters for surface water for acrylonitrile processing
plants in Europe
Table B.1 Local PEC and other emission parameters for surface water for acrylonitrile processing plants in Europe
Site
Processing
capacity
t/y
Process Daily release C, influent WWTP C,effluent
releases
t/y
t/d
mg/l
mg/l
Dilution
factor
1123 2nd river
38681
estuary
1529
river
701
estuary
2000
20
100
10
59
70000
40000
112000
78000
130000
62000
40000
49000
78000
659000
5.750
0.200
0.031
294.000
0.235
0.200
2.134
0.008
0.350
302.908
0.0192
0.0007
0.0001
0.9800
0.0008
0.0007
0.0071
0.0000
0.0012
9.583
0.333
0.052
490.000
35.000
80.000
3.557
0.013
10.000
No
No
Yes
No
Yes
Yes
Yes
Yes
Yes
7.200
0.200
0.002
35.000
0.250
0.100
0.500
0.002
0.250
ABS/SAN
AA
BB (+2)
CC
DD
EE (+D+4)
FF
GG
HH
II
JJ
KK
LL (+HHH)
MM
Total
10300
26000
18000
5000
30000
4000
16000
25000
27000
12000
4500
48000
16000
241800
3.600
4.000
9.000
0.500
0.031
0.500
0.004
0.004
0.010
0.000
5.720
13.200
0.100
36.669
0.0120
0.0133
0.0300
0.0017
0.0001
0.0017
0.0000
0.0000
0.0000
0.0000
0.0191
0.0440
0.0003
6.000
3.800
0.500
0.833
0.052
0.833
0.007
0.007
0.017
0.000
6.200
22.000
0.167
No
Yes
Yes
Yes
Yes
No
Yes
Yes
Yes
Yes
Yes
Yes
Yes
1.160
0.001
0.058
0.100
0.002
0.833
0.009
0.001
0.002
0.000
0.032
0.050
0.050
RCR PEC, sed RCR stp RCR sed
water
mg/kg
0.0064
0.0000
0.0000
0.0499
0.0001
0.0050
0.0050
0.0002
0.0042
0.005
0.000
0.000
0.041
0.000
0.004
0.004
0.000
0.003
0.0092
0.0028
0.0028
0.0527
0.0029
0.0078
0.0078
0.0030
0.0070
0.0081
0.0028
0.0028
0.0438
0.0029
0.0069
0.0069
0.0029
0.0063
0.54
0.17
0.17
3.10
0.17
0.46
0.46
0.17
0.41
0.0076
0.0023
0.0023
0.0436
0.0024
0.0065
0.0065
0.0024
0.0058
n.a.
n.a.
0.00
n.a.
0.05
0.02
0.10
0.00
0.05
0.60
0.18
0.18
3.46
0.19
0.51
0.51
0.19
0.46
0.0008
0.0000
0.0058
0.0007
0.0000
0.0001
0.0000
0.0000
0.0002
0.0000
0.0032
0.0003
0.0004
0.001
0.000
0.005
0.001
0.000
0.000
0.000
0.000
0.000
0.000
0.003
0.000
0.000
0.0036
0.0028
0.0086
0.0035
0.0028
0.0029
0.0028
0.0028
0.0030
0.0028
0.0060
0.0031
0.0032
0.0035
0.0028
0.0076
0.0034
0.0028
0.0029
0.0028
0.0028
0.0030
0.0028
0.0054
0.0031
0.0031
0.21
0.17
0.51
0.20
0.17
0.17
0.17
0.17
0.18
0.17
0.35
0.18
0.19
0.0030
0.0023
0.0071
0.0029
0.0023
0.0024
0.0023
0.0023
0.0025
0.0023
0.0050
0.0026
0.0027
n.a.
0.00
0.01
0.02
0.00
0.17
0.00
0.00
0.00
0.00
0.01
0.01
0.01
0.24
0.19
0.56
0.23
0.18
0.15
0.19
0.18
0.16
0.18
0.39
0.21
0.21
23
Fibre
B (scenario 2)
C (scenario 2)
D (+EE+4)
E
F
G
H
J
K
Total
C, water C water. PEC, water PECwater
annual
annual
mg/l
mg/l
mg/l
mg/l
estuary
river
estuary
sea
sea
APPENDIX B
Table B.1 continued overleaf
1400
30
10
151
1529
7213
573
818
10
10
10
156
125
Site
Processing Processing Daily C, influent
capacity
release release
WWTP
C,effluent Dilution
factor
C, water C water PEC, water PECwater
annual
annual
t/y
t/y
t/d
mg/l
NB COPOLYMERS
AAA
4500
BBB
1200
CCC
1100
8.139
5.260
0.028
0.0271
0.0175
0.0001
50.000
0.047
No
Yes
Yes
11.760
5.800
0.005
DDD
EEE
FFF
1500
10450
12000
0.090
3.150
2.700
0.0003
0.0105
0.0090
0.150
5.250
4.500
Yes
No
Yes
0.018
5.250
0.050
14800
10
4400
600
3.200
13.200
0.0107
0.0440
5.333
22.000
Yes
Yes
4.000 0.0133
39.767
2.480
Yes
0.050
0.100
0.008
156
10
0.0000
0.000
Yes
0.000
10
0.0001
0.0000
0.0000
1.000
0.000
0.000
Yes
Yes
Yes
0.100 150000
river
0.000
500 estuary
0.000
10
GGG
HHH (+LL)
JJJ
Total
10000
45750
24
ACRYLAMIDE + ADIPONITRILE
L
39000
0.000
M
40000
0.030
N
161000
0.000
O
23000
0.000
Total
13.565
mg/l
1250
sea
24570
10
10
10
sea
RCR
PEC, sed RCR stp RCR sed
mg/l
mg/l
mg/l
mg/l
water
mg/kg
0.0094
0.0002
0.0005
0.008
0.000
0.000
0.0122
0.0030
0.0034
0.0105
0.0030
0.0033
0.72
0.18
0.20
0.0101
0.0025
0.0028
n.a.
1.16
0.00
0.80
0.20
0.22
0.0018
0.0004
0.0050
0.001
0.000
0.004
0.0046
0.0032
0.0078
0.0043
0.0031
0.0069
0.27
0.19
0.46
0.0038
0.0026
0.0065
0.00
n.a.
0.01
0.30
0.21
0.51
0.0050
0.0006
0.004
0.001
0.0078
0.0035
0.0069
0.0033
0.46
0.20
0.0065
0.0029
0.01
0.02
0.51
0.23
0.0008
0.001
0.0036
0.0035
0.21
0.0030
0.00
0.24
0.0000
0.000
0.0028
0.0028
0.17
0.0023
0.00
0.18
0.0000
0.0000
0.0000
0.000
0.000
0.000
0.0028
0.0028
0.0028
0.0028
0.0028
0.0028
0.17
0.17
0.17
0.0023
0.0023
0.0023
0.02
0.00
0.00
0.18
0.18
0.18
EU RISK ASSESSMENT - ACRYLONITRILE
Table B.1 continued Local PEC and other emission parameters for surface water for acrylonitrile processing plants in Europe
263000
0.030
Where a production facility and further processing facility(s) are located at the same site, the production figure in column 2
is for the processing site only, but emissions relate to all facilities at the site (as in 4 (+D+EE)
p.a.release / 300 = daily release t/d
[Daily release (t/d) / STP volume (default 2,000,000 l/d)] x 1,000,000,000 (convert t to mg) = C, influent mg/l
C, effluent = C, influent * fraction to water (EUSES 0.116). This accounts for fraction of 0.85 being degraded, 0.0324 discharged to air, and a fraction of 0.00132 in sludge.
Note that the fraction effluent degraded in STP of 0.85 is from EUSES for 'ready biodegradable'.
For site KK, C, effluent = C, influent/22.5*0.116, since the acrylonitrile waste stream is further diluted by other aqueous waste (40 m3 in 900 m3) before discharge into WWTP.
For site JJJ, C, effluent = C, influent/35*0.116, for the same reason as cited for site KK
The fraction to water (less that lost to air and sludge) has only been applied to sites which have been reported to have an STP.
For other sites the C, effluent = C influent.
It was only necessary to apply these fractions to sites which had not provided actual effluent concentrations.
C, effluent / dilution factor (default 10) = C, water.
C water + PEC regional = PEC water (PEC regional (EUSES) = 0.0028)
C water * 300/365 = C, water annual
RCR = PEC/PNEC
PNECwater = 0.017
SUMMARY, 2004
PEC sediment = (0.95/1150)*1000*PECwater = 0.8260869 * PECwater
PNEC sediment = 0.0126 (Section 3.2.1.4)
Site B, Scenario 2 = discharge to main river via 100 m canal
Site C, Scenario 2 = dilution factor proposed by industry
Appendix C Local PEC and other emission parameters to air for acrylonitrile production plants in Europe
Table C.1 Local PEC and other emission parameters to air for acrylonitrile production plants in Europe
Site
25
Production Released Daily relea
t/y
t/y
t/d
1
0.004
120500
1.235
2 (+BB)
0.041
190000
12.400
3
0.017
85000
5.000
4 (+D+EE) 300000
0.011
3.200
5
0.863
280000 259.000
6
0.000
60000
0.054
7
0.008
110000
2.300
8
0.007
105000
2.000
Total
1250500
283
Note
E,air E,effluent E air STP C, air C air ann. PEC, air PECair,ann
Kg/d
mg/l
kg/d mg/m3
mg/m3 mg/m3
mg/m3
4.12
0.0032 0.0011
0.001
0.001
0.001
0.1000
0.0000 0.0006
0.000
0.001
0.001
99.00
0.0013
16.67
0.0036
0.0001 0.0046
0.004
0.005
0.005
10.67
0.0001 0.0030
0.002
0.003
0.003
0.0020
863.33
n.a. 0.2400
0.197
0.240
0.240
5.8000
0.18
0.0120 0.0001
0.000
0.000
0.000
0.3700
7.67
0.0016 0.0021
0.002
0.002
0.002
0.0500
6.67
0.0044
0.0001 0.0019
0.002
0.002
0.002
RCR
air
0.002
0.001
0.009
0.006
0.480
0.000
0.004
0.004
APPENDIX C
Numbers in bold italics are figures provided by industry (emissions provided for all sites)
Where a production facility and further processing facility(s) are located at the same site, the production figure
in column 2 is for the production site only, but emissions relate to all facilities at the site (as in 4(+D+EE)
n.a. = not applicable
p.a.release / 300 = daily release t/d
Indirect emission to air from STP (EUSES) as fraction of effluent = 0.0324.
This only applies to sites with an STP, i.e. sites 1, 2, 3, 4, 6, 7 and 8.
C air = (direct + indirect emissions to air )* 0.000278 (from TGD)
C air + PEC regional = PEC air
PEC regional (EUSES) = 0.0000708 mg/m3
C air * 300/365 = C air, annual
RCR = PEC/PNEC, where PNEC = 0.5 mg/m3
The total release for site 5 represent 62 tonnes from production (monitored) and 197 tonnes from storage (modelled)
Appendix D Local PEC and other emission parameters to air for acrylonitrile processing plants in Europe
Table D.1 Local PEC and other emission parameters to air for acrylonitrile processing plants in Europe
Site
27
FIBRES
B
C
D (+EE+4)
E
F
G
H
J
K
Total
Processing cReleased Daily release
t/y
t/y
t/d
E a E, effluent E air STP
Kg/d
mg/l
Kg/d
C, air C air ann PEC, air PEC air, ann
mg/m3
mg/m3
mg/m3
mg/m3
RCR
air
7.200
0.200
0.002
35.000
0.250
0.100
0.500
0.002
0.250
n.a.
n.a.
0.0001
n.a.
0.0081
0.0032
0.0162
0.0001
0.0081
0.013
0.019
0.000
0.143
0.024
0.005
0.038
0.012
0.015
0.011
0.016
0.000
0.117
0.020
0.004
0.031
0.010
0.012
0.0130
0.0190
0.0001
0.1428
0.0244
0.0047
0.0382
0.0124
0.0149
0.0107
0.0156
0.0001
0.1174
0.0200
0.0039
0.0314
0.0102
0.0123
0.117 116.67
10300
35.000
0.078 99.00
26000
23.500
0.003
3.33
18000
1.000
0.010 10.00
5000
3.000
0.010 10.33
30000
3.100
0.014 14.33
4000
4.300
GG
0.243 243.0
16000
73
HH
0.005
4.83
25000
1.450
II
0.002
1.95
27000
0.585
JJ
0.057 56.67
12000
17.000
KK
0.037 36.67
4500
11.000
LL (+HHH)
0.018 18.33
48000
5.500
MM
0.000
0.00
16000
0.000
Total
241800
178.435
Notes on Appendix 1 4 are provided on the following page
Table D.1 continued overleaf
1.160
0.001
0.058
0.100
0.002
0.833
0.009
0.001
0.002
0.000
0.032
0.050
0.050
n.a.
0.0000
0.0019
0.0032
0.0001
n.a.
0.0003
0.0000
0.0001
0.0000
0.0010
0.0016
0.0016
0.032
0.0006
0.001
0.003
0.003
0.004
0.068
0.001
0.001
0.016
0.010
0.005
0.000
0.027
0.000
0.001
0.002
0.002
0.003
0.056
0.056
0.000
0.013
0.008
0.004
0.000
0.0325
0.0007
0.0010
0.0029
0.0029
0.0041
0.0676
0.0014
0.0006
0.0158
0.0103
0.0052
0.0001
0.0267 0.0650
0.0006 0.0013
0.0008 0.0020
0.0024 0.0057
0.0024 0.0059
0.0033 0.0081
0.056 0.13525
0.0556 0.0028
0.0005 0.0012
0.0130 0.0316
0.0085 0.0205
0.0043 0.0103
0.0001 0.0001
ABS/SAN
AA
BB (+2)
CC
DD
EE (+D+4)
FF
14.000
20.400
0.085
154.000
26.200
5.000
41.175
13.300
16.000
290.160
0.0261
0.0379
0.0003
0.2856
0.0487
0.0094
0.0765
0.0248
0.0298
APPENDIX D
0.047 46.67
0.068 68.00
0.000
0.28
0.513 513.33
0.087 87.33
0.017 16.67
0.137 137.25
0.044 44.33
0.053 53.33
70000
40000
112000
78000
130000
62000
40000
49000
78000
659000
AAA
BBB
CCC
DDD
EEE
FFF
GGG
HHH (+LL)
JJJ
Total
4500
1200
1100
1500
10450
12000
4400
600
10000
45750
21.600
0.018
0.005
1.000
0.600
1.100
20.200
5.500
4.000
54.023
28
ACRYLAMIDE + ADIPONITRILE
L
39000
4.500
M
40000
1.500
N
161000
95.000
O
23000
0.053
Total
263000 101.053
Note
0.072
0.000
0.000
0.003
0.002
0.004
0.067
0.018
0.013
72.00
0.06
0.02
3.33
2.00
3.67
67.33
18.33
13.33
11.760
5.850
0.005
0.018
5.250
0.050
0.050
0.100
0.008
n.a.
0.1895
0.0002
0.0006
n.a.
0.0016
0.0016
0.0032
0.0003
0.020
0.000
0.000
0.001
0.001
0.001
0.019
0.005
0.004
0.016
0.000
0.000
0.001
0.000
0.001
0.015
0.004
0.003
0.0201
0.0001
0.0001
0.0010
0.0006
0.0011
0.0188
0.0052
0.0038
0.0165
0.0001
0.0001
0.0008
0.0005
0.0009
0.0155
0.0043
0.0031
0.0402
0.0003
0.0002
0.0020
0.0013
0.0022
0.0376
0.0103
0.0076
0.015 15.00
0.005
5.00
0.317 316.67
0.000
0.18
0.000
0.100
0.000
0.000
0.0000
0.0032
0.0000
0.0000
0.004
0.001
0.088
0.000
0.003
0.001
0.072
0.000
0.0042
0.0015
0.0881
0.0001
0.0035
0.0012
0.0724
0.0001
0.0085
0.0029
0.1762
0.0002
EU RISK ASSESSMENT - ACRYLONITRILE
Table D.1 continued Local PEC and other emission parameters to air for acrylonitrile processing plants in Europe
Numbers in bold italics are figures provided by industry (emissions were provided for all sites)
Where a production facility and further processing facility(s) are located at the same site, the production figure in column 2
is for the processing site only, but emissions relate to all facilities at the site (as in D (+4+EE)
p.a.release / 300 = daily release t/d
Indirect emission to air from STP (EUSES) = fraction 0.0324.
This only applies to sites with STP; i.e. D, F, G, H, J, K, BB, CC, DD, EE, GG, HH, II, JJ, KK, LL, MM, BBB,CCC,
DDD, FFF, GGG, HHH, JJJ, K, M, N, O.
C air = (direct + indirect emissions to air )* 0.000278 (from TGD)
C air + PEC regional = PEC air
PEC regional (EUSES) = 0.0000709 mg/m3
The total release for site N represent 62 tonnes from production (monitored) and 54 tonnes from storage (modelled)
SUMMARY, 2004